In AD patients, deposition of Aβ amyloid plaques and tau hyper-phosphorylation will drive a reduction at RNA and protein level of OX1R, OX2R and GPR103 which could worsen not only symptoms of weight loss and dysregulation of the sleep wake cycle but also confer a loss of neuroprotection through signalling pathways including ERK1/2; thus exacerbating the symptoms of the disease. The gene discussed is HCRTR2; the disease is Alzheimer disease.